Evidence map›Paper›PMID 37191999›Full record

ArticleJCI insight2023

Regulatory T cells are paramount effectors in progesterone regulation of embryo implantation and fetal growth.

Ella S Green, Lachlan M Moldenhauer, Holly M Groome, David J Sharkey, Peck Y Chin, Alison S Care, Rebecca L Robker, Shaun R McColl, Sarah A Robertson

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
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  8. Distinct macronutrient ratios optimize offspring survival, growth, and maternal glucose tolerance across mouse reproduction.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Review
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  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Ella S GreenRobinson Research Institute, School of Biomedicine, and.
Lachlan M MoldenhauerRobinson Research Institute, School of Biomedicine, and.
Holly M GroomeRobinson Research Institute, School of Biomedicine, and.
David J SharkeyRobinson Research Institute, School of Biomedicine, and.
Peck Y ChinRobinson Research Institute, School of Biomedicine, and.
Alison S CareRobinson Research Institute, School of Biomedicine, and.
Rebecca L RobkerRobinson Research Institute, School of Biomedicine, and.
Shaun R McCollSchool of Biological Sciences, University of Adelaide, Adelaide, South Australia, Australia.
Sarah A RobertsonRobinson Research Institute, School of Biomedicine, and.
Robinson Memorial Hospital · USThe University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progesterone (P4) is essential for embryo implantation, but the extent to which the pro-gestational effects of P4 depend on the maternal immune compartment is unknown. Here, we investigate whether regulatory T cells (Treg cells) act to mediate luteal phase P4 effects on uterine receptivity in mice. P4 antagonist RU486 administered to mice on days 0.5 and 2.5 postcoitum to model luteal phase P4 deficiency caused fewer CD4+Foxp3+ Treg cells and impaired Treg functional competence, along with dysfunctional uterine vascular remodeling and perturbed placental development in midgestation. These effects were linked with fetal loss and fetal growth restriction, accompanied by a Th1/CD8-skewed T cell profile. Adoptive transfer at implantation of Treg cells - but not conventional T cells - alleviated fetal loss and fetal growth restriction by mitigating adverse effects of reduced P4 signaling on uterine blood vessel remodeling and placental structure and by restoring maternal T cell imbalance. These findings demonstrate an essential role for Treg cells in mediating P4 effects at implantation and indicate that Treg cells are a sensitive and critical effector mechanism through which P4 drives uterine receptivity to support robust placental development and fetal growth.

Indexed as

ProgesteroneT-Lymphocytes, RegulatoryAnimalsEmbryo ImplantationFemaleFetal DevelopmentFetal Growth RetardationHumansMicePlacentaPregnancyProgesteroneEmbryonic developmentReproductive BiologyT cellsTolerance

Identifiers

PMID37191999
PMCPMC10393240
OpenAlexW4376643114

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.